Quick questions on Apoptosis, disruption to the cell cycle and cancer: VCE Biology Unit 1

Apoptosis is programmed cell death: a regulated, energy-requiring process by which the cell dismantles itself in a controlled way. It is essential for development, tissue homeostasis and elimination of damaged or infected cells.

Extrinsic (death receptor) pathway. Triggered by external signals binding to death receptors on the plasma membrane (such as Fas binding FasL on a cytotoxic T cell). The death-receptor complex activates caspase-8 (initiator), which activates caspase-3 (effector).

Triggered by external signals binding to death receptors on the plasma membrane (such as Fas binding FasL on a cytotoxic T cell). The death-receptor complex activates caspase-8 (initiator), which activates caspase-3 (effector).

Triggered by internal damage signals (such as severe DNA damage detected by p53, or oxidative stress). The mitochondrial outer membrane becomes permeable, releasing cytochrome c into the cytoplasm. Cytochrome c binds Apaf-1 to form the apoptosome, which activates caspase-9 (initiator), which activates caspase-3 (effector).

Normal genes whose products promote cell division (growth factors, growth-factor receptors, signal-transduction proteins, cyclins). A gain-of-function mutation turns a proto-oncogene into an oncogene, producing a hyperactive or constantly-on version that pushes the cell to divide even without a normal signal. Examples: Ras (a signalling switch stuck "on"); HER2 (a growth-factor receptor over-expressed in some breast cancers).

Normal genes whose products inhibit cell division or trigger apoptosis when damage is detected. They act as brakes. A loss-of-function mutation removes the brake.

Describe two morphological features of a cell undergoing apoptosis that distinguish it from a cell undergoing necrosis. [2 marks]

A tumour sample shows mutations in two genes: TP53 and BCL2. Predict how each mutation affects apoptosis and explain how this contributes to tumour growth. [3 marks]

Refer to the role of caspases in cell death. (a) State the difference between initiator and effector caspases. (b) Describe how the intrinsic (mitochondrial) pathway activates caspase-9.